Fig. 4

apoEV-MTA1 promotes radioresistance by inducing cellular dormancy. (A) Western blot analysis assessing the expression levels of MTA1 in EVs from CC cells infected with either the MTA1 knockdown virus (shMTA1) or the control virus (shNC). (B) Grayscale analysis of MTA1 expression in the indicated cells and corresponding EVs using western blotting. *P < 0.05. ns, no significant difference. (C) Detection of MTA1 levels in CC cells after 48-hour pretreatment with the specified EVs, analyzed by western blot. (D) FACS analysis of Annexin V/PI staining in SiHa (D) and HeLa (E) cells treated with either shMTA1-apoEVs or shNC-apoEVs. Radiation sensitivity was assessed through colony formation assays. (F) Decreased clonogenic formation in SiHa and (G) HeLa cells treated with shMTA1-apoEVs compared to shNC-apoEVs. (H) qRT-PCR analysis of key dormancy regulators (DEC2, NR2F1, p27, Bim-1) in CC cells treated with either shMTA1-apoEVs or shNC-apoEVs. (I) Western blot analysis showing NR2F1 expression levels in CC cells after treatment with shMTA1-apoEVs or shNC-apoEVs. (J) Glucose consumption analysis in CC cells after incubation with shMTA1-apoEVs or shNC-apoEVs for 48 h. (K) FACS analysis of cell cycle progression in CC cells after 48-hour incubation with shMTA1-apoEVs or shNC-apoEVs